Overview: Gastric cancer is one of the most common malignant tumors in China The incidence rate among the first types of cancer, each year about 17 million people died of stomach cancer, almost all cancer deaths in nearly 1 / 4, and each year more than 20,000 new cancer patients have come out, stomach cancer is indeed a serious threat to people's health diseases. Gastric cancer can occur at any age, but the more common 40 to 60 years, more men than women about 2:1. Gastric cancer can occur in any part of the stomach, but more common in the gastric antrum, lesser curvature of the stomach in particular. Average life expectancy without treatment is about 13 months.[Cause]
gastric cancer is caused by what the?
(a) the cause of gastric cancer etiology has not yet been fully elucidated, a large number of research data shows that the incidence of gastric cancer is the result of many factors, summarized as follows. 1 stomach through diet and external factors outside world, some cancer-causing factors can play a role in cancer. (1) N-nitroso compounds: in 1956, Magee and other proven carcinogenic dimethylnitrosamine, and successfully induced in the rat liver. Later scholars have confirmed more than 200 species of nitroso compounds can cause cancer in animals. Some animals can also be induced in a variety of gastric cancer. In humans, nitrosamine precursors in gastric juice - nitrite content and the prevalence of gastric cancer has a very clear correlation. Now known carcinogenic nitrosamine compounds have two categories: ① N-nitrosamines; ② N-nitrosated amide. The former are mostly volatile, by microsomal activation of cell damage the genetic material DNA in order to show carcinogenic effects; which can directly damage DNA, and hence more closely related to gastric cancer. N-nitroso compounds in nature is widespread, pickled foods, sauerkraut with N-nitroso compounds. Food directly into the body can be said with exogenous. And its precursors, such as secondary amines and nitrite there is more extensive in nature, into the human body in the appropriate pH (pH1 ~ 3) by chemical processes under, or under the action of bacteria by the formation of the biosynthesis of nitroso compounds, called endogenous. Biosynthesis is more important. This catalytic synthesis of a variety of bacteria, the stomach environment is conducive to the growth of these bacteria, such as low stomach acid, etc. may indirectly promote synthesis of N-nitroso compounds. Dietary factors influence the incidence of gastric cancer, cancer researchers have been hampered by the attention. Possible for the regular consumption of dietary carcinogens smoke, roasting food (including benzopyrene) or pickled foods, sauerkraut (including N-nitroso compounds). Recent studies have also proposed protective factors, such as milk, animal protein, fresh vegetables and some fruits. Recently, Japan and the United States the decline in the incidence of gastric cancer have been attributed to improvements in diet, but the relationship between diet and cancer research and cancer-causing mechanism is extremely complex. Foods may play a direct role in both carcinogens, either naturally or in the food cooking, processing, storage generated in the process; food intake of the body in the body after a number of factors may also be formed under the action of carcinogens. In the carcinogenic process, some starting material plays the role of carcinogens, tumor promoters or tumor suppressor plays some role, but also with the complexity of the human body's metabolism, biotransformation processes are intertwined, it is difficult from the These complex factors found positive links. Experimental data can be used to evaluate the dietary and metabolic factors in human gastric cancer in the role, as its results are consistent with epidemiological evidence, the result was convincing. Comprehensive survey of China's gastric cancer epidemiology group of domestic high-and low-incidence area of gastric cancer and diet survey showed that close. In toxin-induced rat liver Aspergillus versicolor experiments, had seen the occurrence of gastric adenocarcinoma. The main non-staple food from the survey area and can be detected in patients with gastric Aspergillus versicolor and Aspergillus nidulans and other fungi, in areas of high cancer detection rate is clearly higher than the low-prone areas, can prompt a grain mold-related risk of gastric cancer factors. High-salt food salt is considered to be another gastric cancer risk factors. High incidence of gastric cancer in China residents to 9kg salt intake per person per year or more, and residents in areas with low salt intake, compared with 4 ~ 7.5kg. Comparative survey also found that in areas of high gastric cancer more than a simple food species, and areas with low food variety, fresh vegetables, legumes and animal protein intake also, and this may indicate that the balance between gastric cancer and loss of nutrients. In addition, the survey prompted fresh vegetables to adjust food intake and gastric cancer mortality was negatively correlated with that of fresh vegetables is a protective factor. Fresh vegetables rich in vitamin A, C and minerals. Vitamin A in epithelial regeneration and to maintain its normal function of the vitamin C can block the amine nitrite and nitroso compounds synthesized in the stomach. Iron deficiency has been confirmed with the Plummer-Vinson syndrome, the latter with the occurrence of esophageal and gastric cancer, iron deficiency and thus indirectly related to the incidence of gastric cancer. (2) H. pylori (helicobacter pylori, HP) infection: in recent years generally agreed that H. pylori infection and gastric cancer pathogenesis. 1994, WHO has listed it as the first class of gastric cancer risk factors. Domestic and international epidemiological data indicate that the incidence of gastric cancer was positively associated with HP infection, HP infected gastric cancer risk than non-infected persons increased 6 times. Also found high incidence of gastric cancer, HP infection early age. Children under the age of 10 of China's Lanzhou infection rates reached 40% to 50%, Changle City, Fujian, children under 5 years were as high as 50%, significantly higher than the low-incidence areas. Rarely in normal gastric mucosa in Helicobacter pylori isolated, but with increasing gastric mucosa, Helicobacter pylori infection increased; determination of the serum of gastric cancer patients and found significantly higher rates of Helicobacter pylori antibodies for cancer the risk factors. HP in gastric cancer, the mechanism is in many ways. HP itself can produce some toxic metabolic substances, such as urea, phospholipids, enzymes, these substances can reduce the acidity of the local environment and lead to epithelial cell damage, resulting in chronic atrophic gastritis; other HP infection causes gastric inflammatory cell infiltration, the oxygen increase in free radicals and a variety of cytokine release, leading to DNA damage and apoptosis. A number of studies show that the HP infection in gastric epithelial cell apoptosis index was significantly increased. Epithelial cells to stimulate cell proliferation or lead to gastric atrophy, gastric cancer is a major part. HP infection in patients with gastric various reports vary, in addition to sampling and inspection methods and different populations may still on the foreign stage of disease and gastric cancer, histological type, lesion related. Asaka, etc. found in HP-positive early gastric cancer was 93%, significantly higher than healthy controls, also higher than in patients with advanced gastric cancer. Some people think that intestinal-type early gastric HP infection rate higher than the diffuse type early gastric cancer, but there was no significant difference between the two reports. Menegtti other analyzed 307 cases of non-cardiac region (antrum, gastric body, gastric) cancer patients with HP serum antibody positive rate of 81% to 83%, no significant differences between, but significantly higher than cardiac patients. That live parts with HP and gastric inflammation. Parsonnet HP made the three hypotheses lead to gastric cancer: ① bacterial metabolic products directly into the gastric mucosa. ② HP's DNA integration host cell DNA. ③ cause inflammation, and then produce genotoxic effects. Currently a large number of research data to support the third hypothesis, that chronic active gastritis - chronic atrophic gastritis - intestinal metaplasia - dysplasia - the model of development of gastric cancer. It is well established, multi-atrophic gastritis and HP infection; HP's relationship with intestinal metaplasia are also many studies, Fontham HP infection and other intestinal metaplasia found in the risk of non-infected 4.7-fold; a stomach with a PCR assay mucosa of HP's research showed that the detection rate of dysplasia HP 89.5%, significantly higher (27.5%). Recananen 17 cases of HP-positive dysplasia treatment, 7 were removed and inflammation improved with HP dysplasia disappeared. Thus, most scholars believe that HP is a major role in cancer initiation factor the initial stage, that is, in active gastritis, atrophic gastritis and intestinal metaplasia plays a major role in the development, at a later stage whether the work is not yet clear. Generally believed that gastric cancer from exposure to the cause of about 10 to 20 years, and from the development of gastric cancer to diagnosis of gastric cancer and it takes a long time. Studies have shown that HP can make epithelial cell proliferation activity, both with bacterial toxins (uremic enzyme, phospholipase enzymes), but also with the host response (cytokines such as TNF, interferon, etc.). Recent studies have shown that HP can promote apoptosis in gastric epithelial cells stimulate compensatory proliferation. Once the inhibition of apoptosis, cancer may occur. The other two hypotheses on the Parsonnet data was small. Recently been suggested from chronic gastritis to gastric cancer sequence theory that chronic gastritis - atrophy - intestinal metaplasia - dysplasia - gastric cancer, and HP infection is the most important cause of chronic gastritis, gastric cancer, with the progressive development of chronic gastritis a multi-step, multi-factor process. HP is an important gastric cancer risk factor, with a variety of host factors and external factors influence each other, eventually leading to gastric cancer (Figure 1). (3) fungi: fungal toxin-induced gastric adenocarcinoma or gastric precancerous lesions. Aspergillus has proven complex and its metabolites N-nitroso compounds with a synergistic carcinogenic effects. Some fungi can also be synthesized N-nitrosamines. Long-term consumption of moldy food may be an important factor in cancer. (4) Schistosomiasis: Schistosomiasis stomach cancer rate has been reported up to 50% to 75%. Has not yet extracted from schistosome eggs carcinogens, whether mechanical stimulation or egg toxins, yet to be confirmed. (5) geographical factors: the epidemiology of gastric cancer worldwide survey of different regions and ethnic groups there are significant differences in the incidence of gastric cancer. These differences may be related to genetic and environmental factors. Some information on gastric cancer, mainly in the high latitudes, farther from the equator of the country, the higher the incidence of gastric cancer. Also has information that its incidence and coastal factors. There are different factors in eating habits should also be considered in the geochemical factors and environmental carcinogens may be present. Epidemiology of gastric cancer study group of China's comprehensive national cancer has been investigated by high-prone areas, such as the Hexi Corridor in Qilian Mountain stream river, the Yellow River, Yangtze River, Minjiang River Estuary, Mulan downstream and the southern section of the Taihang Mountains and other places, found that in addition to the southern section of the Taihang Mountains metamorphic rocks, the other volcanic rocks, high peat, local or deep side of the fault, the water Ca2 / SO4 ratio is small, and nickel, selenium and cobalt content. Gastric cancer study group also investigated the low-prone areas, such as the Yangtze River and Pearl River and other places, find the area of limestone areas, no deep faults, water Ca2 / SO4 ratio of large, nickel, selenium and cobalt content is low. Volcanic rocks are known to contain 3,4 - benzopyrene, some as high as 5.4 ~ 6.1μg/kg, peat and other organic nitrogen precursors with higher levels of nitrosamines, the gastric mucosa prone to injury. In addition, selenium and cobalt can cause stomach damage, nickel can promote 3,4 - benzopyrene of carcinogenic effects. Whether the above factors for the formation of the geographical environment of these cancer-prone areas of domestic reasons, it is worth further exploration. (6) Other factors: a large survey data show that the social, economic, geographical, psychological and dietary behaviors and habits in the pathogenesis of gastric cancer have a certain effect. High-salt diet, smoking also has a certain relationship. It has been reported in patients with gastric cancer blood, hair and tissue chromium, cobalt, selenium, copper, manganese content and the ratio of change may be related to soil-related, but the lack of accurate information on dose-effect relationship. (2) internal factors (1) genetic factors and genetic variation: tendency of familial aggregation of gastric cancer, gastric cancer incidence in family members of patients in general 2 to 4 times. In the ANO blood different populations between gastric cancer incidence may be different in different racial there are differences, some statistical Type A's cancer incidence rate than other blood types were 20%, but there are some reports that the different blood type of gastric cancer incidence there is no difference. In recent years, the incidence of gastric cancer was the relationship with HLA, pending further conclusions. Survey data indicate that genetic factors play an important role in gastric cancer. In recent years, found that gastric cancer and precancerous lesions of cell chromosomal abnormalities, mostly in the number of chromosomes in aneuploid; in structural chromosomal rearrangements can occur, fracture, loss and other abnormalities. Recent discovery, there are a variety of normal human cells, proto-oncogenes and anti-cancer genes, collectively known as cancer-related genes. Are on a sequence of DNA. Their normal differentiation in cell growth and individual development, not only harmless, but also has biological functions. Carcinogenic effect of different factors, cancer-related gene mutation and loss of normal physiological role in the carcinogenic potential function is activated. Which activation of oncogenes known cancer genes. Studies have shown that a single oncogene activation or lack of anti-cancer gene mutation causes cells to cancer, cancer-related genes to be more multi-step multi-stage synergy to make cells malignant transformation. Cancer-related genetic variation of different tumor types and different ways, each mutant gene only in the carcinogenic process may play a role in one step. Therefore, tumor formation requires the development of a long process, but also by a variety of factors both inside and outside the body. With nearly 20 years to the theory of modern cell and molecular biology and technology, biological engineering, the use of new technologies such as cloning and sequence analysis, DNA recombination, hybridization, monoclonal antibodies and ELISA techniques, PCR, restriction fragment length polymorphism analysis and gene transfection of gastric carcinogenesis, etc. a lot of research work has been clear for cancer genes met, EGFR, erB2, akt-2 and ras, the main active way point mutation, amplification, methylation, overexpression, rearrangement and exogenous insertion, such as met, EGFR, erB2, akt-2 amplification or overexpression, H-ras gene codon 12 mutations. Anti-cancer gene p53, p16, Rb, nm23 and APC, in order to mainly point mutations and deletions, such as p53 174 and 280 codon mutations, APC exon 11 deletion, Rb deletion and rearrangement. These abnormal genes in cancer cells affect different stages of the process of dysplasia, cancer cell differentiation, invasion and metastasis. But is not yet clear and specific sequence of genetic changes in chromosomal changes. Now clearly met, ras gene overexpression in cancer early, met, EGFR, erB2, akt-2 amplification and rapid growth of the tumor, in advanced gastric cancer, met-2, erB2 amplification abusers who have lymph node metastasis and vascular thrombosis. nm23, p16 gene deletion or low expression levels and p53 point mutations or deletions were poorly differentiated cancer cells, invasion and metastasis ability, it is associated with the malignant phenotype. Intestinal metaplasia and dysplasia found that p53 mutations may be cancer indicators. APC gene deletions more common intestinal type gastric cancer and its point mutations more common in diffuse-type gastric cancer, Rb gene deletions and rearrangements seen in mucinous adenocarcinoma. The normal p53 gene into p53 abnormal cells can inhibit the cell proliferation. DNA methylation is regulated at the transcriptional level of genes one way, methylation of gene activity after reduction, is to maintain the genetic stability of cells, an important factor. In tumor and transformed cells, the total genome, and certain cancers or reduce the level of gene methylation patterns change. Shanghai Institute of Digestive Disease application 3H-SAM incorporation and HPLC method and Southern blot analysis confirmed that human gastric cancer cells, the total genome and cancer-related gene methylation levels. And precancerous lesions of half of the c-myc and H-ras gene hypomethylation. And confirmed that the total level of gene methylation in the lower, the worse the degree of cell differentiation. (2) the imbalance of apoptosis and proliferation: the balance of normal tissue is mainly within the cell proliferation and death balance, too much growth is too little cell death and excessive breeding results. The cell death process of the disorder is closely related with the formation of tumors. Cell death has been known there are two ways: necrosis and apoptosis. Apoptosis is a physiological, highly programmed, automated cell death. To cell shrinkage, chromatin concentration, apoptotic body formation and degradation of nuclear DNA characteristic features. Cells not only maintain a stable number of cells within the organization functions, and can maintain the accuracy of genotype, phenotype variation to reduce, eliminate changes in the genotype. Thereby preventing the occurrence of cancer. Therefore, the abnormal cells may be an important element of the process of carcinogenesis. Now clear that regulation of apoptosis in a variety of factors, in strict accordance with procedures. Which may be tumor suppressor gene p53-mediated apoptosis. Under normal circumstances, DNA is damaged, p53 gene product accumulation can induce cells to enter G1 phase and fix it, repair fails, p53 can induce apoptosis gene products in order to prevent a cancer cell mutations tend to survive . P53 mutations and loss of the monitoring function, it can lead to cell mutations and genetic instability and chromosomal aberrations, it may eventually lead to cancer. Apoptosis program, another key gene bcl-2 oncogene and his family have the role of inhibition of cell death, bcl-2 was mainly localized in the nuclear membrane, endoplasmic reticulum and mitochondrial outer membrane. In the carcinogenic process, it is not by accelerating cell division, but prolong cell survival. In addition, there are tumor suppressor genes involved in c-myc, the expression of the gene product may be given cell are two options: death and proliferation. Selected direction is subject to additional stimuli, such as bcl-2 can inhibit c-myc, accelerated cell proliferation, may induce cancer. Involved in induction of apoptosis were the bax, bik, bcl-xs, Fas protein and other genes. In addition, a series of receptor activation can trigger apoptosis. Secreted by a variety of cells such as a growth factor that is transforming growth factor β1 (TGF β1) receptors. (3) immune dysfunction: the incidence of tumor development and metastasis and immune status are closely related. Specific immunization and non-specific immune mechanism is strong, some tumors grow slowly, not spread, and even natural healing. Suppressed immune function, damaged or defective, and the rapid development of tumor-prone, easy to transfer. Has been confirmed in vivo immune effects on elimination of carcinogenic factors also play an important role. There are a variety of cancer cell surface antigens, called cancer-associated antigen. Immunogenicity, although weak, but still start the host immune response to bacterial immune-based, humoral immunity is also involved. First, activate the gastric cancer antigen interstitial lymphoid tissue and nearby lymph nodes lymphocytes, immune activity and play a role into the circulation, to a certain extent, affect the biological characteristics and prognosis of gastric cancer. China Medical University Cancer Institute confirmed that the bulky, mass growth, without lymph node metastasis of gastric cancer and nearby lymph nodes within the stromal cells increased immune activity; and diffuse, infiltrative growth, lymph node metastasis, the immune cells increased not obvious. Gastric lymph nodes around the area of cancer in the lymph node T cells have a certain inhibitory effect, while the B lymphocytes within the cancer cells grow in the stomach seems to inhibit proliferation. Early confirmed that the initial tumor effects and immune cells can be induced with tumor growth and enhancement; but in tumor growth over a certain limit, but lower immunity; to be the primary tumor resection, but also to restore immune function. Now known and the immune suppression-related factors include: ① closed factor, which combined with the surface of the tumor antigen - antibody complexes, prevent the formation of new antibodies and immune activity in cells. ② immune function, due to repeated stimulation of tumor-specific antigen immune tolerance appears first, then the immune paralysis, loss of the host immune system monitoring capabilities. The later stage of disease of this phenomenon is more obvious. ③ immunosuppressive α-globin increased beyond physiological concentrations. As the immunological basis of current theory and immunology technology breakthrough, tumor immunology has developed rapidly. The new tumor-associated antigens to discover, the use of hybridoma technology, monoclonal antibodies obtained by the increasing number of lymphokines or cytokines such as interferon, interleukins, colony-stimulating factor, tumor necrosis factor and tumor-killing cells such as natural killer cells, T killer cells, LAK cells and other tumor deepening understanding of the role, not only to promote the cause of understanding of the pathogenesis of gastric cancer and gastric cancer have been or are being used in the diagnosis, prognosis, treatment and prevention. (4) low non-immune protective factors: There is experimental evidence exists in the case of carcinogens, damage to the gastric mucosal barrier and anti-factor interactions and damage factors play an important role in the pathogenesis of gastric cancer. Some of the antioxidant vitamins such as vitamin A, C, E and β-carotene and other anti-cancer effect. Low content of long-term in vivo, enabling tumors may be related to increased activity of oxygen free radicals, cell immune function and intercellular connections of traffic congestion and so on. In recent years, found that folic acid deficiency and the pathogenesis of gastric cancer, because folic acid is one carbon unit donor, and DNA methylation, the lack of time can cause reduce the level of gene methylation, prone to cancer. (5) the role of oxygen free radicals: experiments confirmed that oxygen free radicals in carcinogenesis, tumor promotion and anti-cancer aspects play an important role, it can start cell division, DNA synthesis and can damage the cells, and activation of oncogenes lead to cancer. Under the action of free radicals generated in lipid peroxidation (LPO), make some "carcinogen" into carcinogens, promote cancer. Mitochondrial Mn-superoxide dismutase (Mn-SOD) activity was significantly loss is one of the reasons cancer. Oxygen free radicals may initiate apoptosis is one of the factors. (6) the role of hormones in the digestive tract: gastric cancer have been found there are seven kinds of endocrine cells and gastric cancer cells constitute the nest, infiltration in the stroma, through autocrine or paracrine manner on the cancer's own growth, differentiation, metabolic, histological type and metastasis, etc. play a role. Gastrin has been reported, mainly through cAMP and cAMP-dependent protein kinase (PKA) cancer, and to promote the growth of cancer cells. Found in low concentrations in vitro cell culture gastrin can promote malignant cell growth. Animal experiments have found that gastrin-induced promotion of N-nitrosamines in the role of gastric cancer, especially in the early stages, the main cause of hard cancer. Gastrin can cause gastric cancer diffuse fibrosis, the prognosis is poor. Gastrin disturbance agent - proglumide can inhibit tumor growth and promote the role of gastrin. Bennett and other reports, can be detected in gastric cancer tissues to a transforming growth factor (α-TGF) and growth factor receptors in patients with poor prognosis. Some atypical hyperplasia if this factor is found cancer rates were high. Most observations suggest that estrogen and the growth of gastric stimulation, and androgen inhibition. Marita found that prolactin-positive rate and depth of invasion and lymph node metastasis of gastric cancer was positively correlated with the range. (7) disease factors: It is well established, some of the higher incidence of disease in patients with gastric cancer, it is regarded as precancerous lesions, also known as precancerous condition. Such patients as high risk. Including chronic atrophic gastritis, gastric ulcer, gastric polyps, residual stomach and hypertrophic gastritis. ① chronic atrophic gastritis: chronic gastritis can be divided into superficial, atrophic and hypertrophic three. Atrophic gastritis is now recognized as a precancerous lesion of gastric cancer, especially with gastric polyps or the presence of intestinal metaplasia at the same time more likely. Domestic and international long-term follow-up reports, a history of chronic atrophic gastritis and gastric cancer length and severity of the incidence of the many reports of the disease incidence of stomach cancer about 2% to 10%. Gastritis can be cured, but there may be gradually transformed into atrophic gastritis. Hypertrophic gastritis and gastric cancer has little to do. Atrophic gastritis quite difficult to cure, the organization tends to regeneration, sometimes the formation of polyps, and sometimes cancer. Long-term follow-up track can be found in atrophic gastritis to cancer by up to 10%. Comprehensive survey of our material shows that gastric cancer, gastric cancer high incidence of superficial and atrophic gastritis patients was significantly more than low-incidence area of gastric cancer. High incidence of chronic gastritis patients with fasting gastric analysis showed free acid content decreased, pH, bacteria, NO2, and nitrate-reducing bacteria levels higher detection rate, compared with low-incidence areas were significantly different. Changes in the gastric environment, the extent of lesions and the severity of chronic gastritis positive correlation also shows that patients with chronic gastritis, gastric environment changes, is very conducive to N-nitroso compounds. ② gastric polyps: benign tumors have no malignant potential of gastric, and epithelial malignant adenomas or polyps more opportunities. Villous adenoma type and rare type of stomach polyps rate of up to 15% to 40%, while the most common hyperplastic polyps only 1%. Polyps larger than 2cm in diameter, the increased incidence of cancer. Data reported by X-ray diagnosis of gastric polyps in patients, 20% with a malignant transformation; in gastric polypectomy specimens, see 14% of multiple polyps are malignant, and 9% of single malignant polyps, which Description of the cases diagnosed as gastric polyps are not easily let go. ③ gastric ulcer: gastric ulcer problem has always been understanding of cancer is not uniform. Generally believed that the cancer rate is about 1% to 6%. Most ulcers are marginal and that intestinal metaplasia or dysplasia mucosa related. Can gastric cancer on the issue, reported in gastric carcinogenesis domestic rate of 5% to 10%, especially long history of gastric ulcer and middle-aged patients with a greater chance of cancer, ulcers, or the Ministry of epithelial glands by gastric erosion and erosion occurred in the repeated destruction and regeneration of the chronic stimulation into cancer. ④ remnant stomach: surgical removal of benign gastric antrum and body part, the reduced gastric acid secretion, leading to bile reflux, the formation of the stomach neutral and alkaline environment in the stomach abnormal reproduction of bacteria, promoting nitrite and N- nitro compounds induced cancer, usually occurs in patients over 10 years. China remnant gastric cancer incidence rate of 2% to 5%, have also been reported for more than 10%. Billroth Ⅱ anastomosis than Billroth Ⅰ anastomosis is high. May be related with bile reflux. Many anaerobic bacteria such as gastric juice into the stomach can break down the combination of anti-type primary bile acid, can damage the gastric mucosal barrier and can produce carcinogenic secondary bile acids sequestered, and in the secondary bile acid deoxycholic acid in is a cancer initiation factor, lithocholic acid is a cancer initiation factor and mutagenic materials. These may lead to subsequent occurrence of gastric stump cancer. Remnant gastric cancer occurred in 15 to 20 years after surgery, then the relative risk increased by 3 to 6 times. ⑤ large gastric mucosal folds disease (Menetrier disease): The disease is cancer rate is about 10%. ⑥ bile reflux: Animal experiments have confirmed by bile reflux can induce cancer. Epidemiological survey also found that bile reflux gastritis and gastric cancer was positively related to the mechanism above. 3 intestinal metaplasia and dysplasia from normal gastric mucosa into gastric cancer is a long gradual process, this process occurs in certain transitional lesions as precancerous lesions. Study the formation of these lesions, development, transformation conditions and laws of gastric cancer etiology, pathogenesis and prevention of important links. Is that the gastric intestinal metaplasia and dysplasia are precancerous significance, while the latter is more meaningful. Recent expansion was proposed also has shaped gland cystic nature of precancerous lesions. (1) dysplasia: also known as dysplasia. Is the deviation from the normal gastric epithelial growth and differentiation of pathological changes, including cellular atypia, structural disorder and abnormal differentiation. Common in atrophic gastritis, gastric ulcer edge and gastric cancer tissues. Is recognized as precancerous lesions. Jass will be divided into two types dysplasia that are relevant and incomplete intestinal metaplasia. Pause type Ⅰ level in undifferentiated cells coexist with intestinal adenocarcinoma. Type Ⅱ stop at intermediate level, and often co-exist with poorly differentiated adenocarcinoma of intestinal type. The country will be divided into adenomatous dysplasia type, type and regenerative crypt, which is a lower cancer rate. In recent years, also found that the ball-like dysplasia, and identified closely with the signet ring cell carcinoma; was divided into two subtypes, Ⅰ-type cells to neutral mucus mainly occurred in the stomach and neck glands; Ⅱ type occurred Department of intestinal metaplasia in the glandular crypts. In addition, still found a non-intestinal metaplasia-type dysplasia may be diffuse gastric precancerous lesions. Have yet to find a considerable number of the corresponding gastric precancerous lesions. Current grade dysplasia is not uniform, there is a certain subjectivity. Domestic sub-light in weight 3. Endoscopic follow-up results showed that the cancer rates were: 2.5% mild, moderate 4% to 8%, severe 10% to 83%. In addition, a number of morphometric analysis of gastric mucosa, nuclear DNA content, cell population dynamics, and epithelial cells of the macrophage silver nucleolar organizer region proteins (Ag-NOR) quantitative analysis mused with dysplasia increased and increasing; In addition, some tumor-associated antigens CEA, MG7-Ag, etc., cancer genes and their products such as c-mycP62 and rasP21, P53 tumor suppressor gene abnormalities and other biological markers of the content or the detection rate significantly different from normal gastric mucosa mused that shaped high risk of cancer proliferation. However, these indicators parameter variation, there is overlap between the two groups are difficult to quantify, it is difficult to identify differences between benign and malignant. A large number of clinical observations indicate that dysplasia may not be cancerous, its direction may be three: ① reversed. ② long-term change. ③ from mild to severe, and finally cancer. Only three cases occurred in the conditions and laws have not yet fully elucidated, indicating the direction of its development indicators have not yet found, appropriate treatment needs further study. According to China's comprehensive cancer information obtained by study group, the initial idea of the cause of the following model (Figure 2). (2) intestinal metaplasia: gastric intestinal metaplasia (intestinal metaplasia) refers to the gastric mucosa appeared on the intestinal epithelial similar, but with absorptive cells, goblet cells and Paneth cells, no secretion of neutral mucus secreted protein acidic mucus proteins but there is relatively immature and differentiated way to the intestines and stomach characteristics. Intestinal metaplasia began in the pyloric gland neck cells, pyloric glandular epithelium into the intestinal metaplasia of the epithelium. Occur in the gastric intestinal metaplasia and pyloric gland area, and gradually to the migration department and body extension, the same predilection sites of gastric cancer, and age range to expand. Intestinal metaplasia is common in chronic gastritis, especially atrophic gastritis, gastric ulcer edge and adjacent tissues. Can be divided into three severity: mild, occasional gastric intestinal metaplasia within the tubular cell; moderate, up to about 1 / 2; and severe, and the majority of gastric intestinal metaplasia of duct cell is replaced. According to the intestinal absorption of cell morphology is divided into two types, namely, absorptive cells with well-developed microvilli, cytoplasmic granules without mucus, intestinal epithelial enzymes called completely positive type, on the contrary called incomplete type. And according to their type of mucin secretion into: intestinal-type sialic acid mucin secretion, colonic secretion of oxygen - acetylated sialomucins. In 1979 Jass also found a secreted acid mucin (sulphomucins) of intestinal metaplasia, is a type of incomplete-type intestinal metaplasia of the colon, also known as type Ⅲ intestinal metaplasia. This type of intestinal metaplasia with differentiation of immature, such as a variety of cancer-associated antigen MG7, MGdl, MG3, CEA, CA19-9, sialic acid glycoprotein, Lee antigens and oncogene products rasP21, FasP85 other was higher than normal and other intestinal metaplasia, nuclear DNA content increases, etc., it is closely related with gastric cancer. Intestinal metaplasia reported in the literature by a 10-year follow-up cancer rate of 1.9%. Generally believed that the differentiation of intestinal metaplasia and intestinal-type gastric cancer, recent studies have also revealed some type of stomach cancer and stomach, part of the diffuse-type gastric cancer, may also coexist with a small number of gastric carcinoma and poorly differentiated type tubular epithelial diffuse cancer. (3) expansion of the opposite sex glands: gastric glands expansion can be divided into two kinds of simple and odd, slight expansion of the former glands without atrophy and atypia, focal or isolated distribution, return to normal after treatment. Shaped into a small number of expansion, also known as cystic shaped expansion, the expansion of the gland with severe atrophy, may be associated with dysplasia and intestinal metaplasia. China reports 9.9% rate of cancer, precancerous lesions may be important. In summary, the etiology and pathogenesis of gastric cancer is very complicated, it is carcinogenic by a variety of external factors acting on defective body, or in some genetic background, showed a specific reaction of the carcinogen, after a long period, multi-step formation of malignant disease. Some people think that, although age of onset of gastric cancer in middle age, but carcinogenic effect in puberty has occurred. At present, tend to chronic gastritis - intestinal metaplasia - dysplasia - the incidence of gastric cancer model. (B) any part of the pathogenesis of gastric cancer can happen, the most common gastric antrum (48.8% ~ 52.5%), greater curvature, lesser curvature, anterior, posterior Jieke involvement, followed by the cardia (16.1% 20.6%), gastric body and involving the whole stomach were relatively small (7% ~ 16.6%). Gastric cancer as single, small can also be multiple. Incidence of gastric mucosal epithelium at the start, mostly single-center place, a small number of multi-center occurred. The latter is also not far more evolved due to the integration into a foci, even the formation of double cancer. Foci gradually developed, while the horizontal direction and deep infiltration and proliferation, gradually involving the gastric wall layers or surrounding organs can also be transferred through a variety of ways. Early stage of disease on the efficacy and prognosis greatly. 1 violation of pathologic gastric cancer according to depth, is divided into early and advanced gastric cancer. Does not exceed the depth of invasion of early gastric cancer who said submucosa, invasion to the muscle layer, said mid-stomach, serosal and serosal invasion and advanced gastric cancer than those who said that, in advanced gastric cancer together with advanced gastric cancer. (1) early gastric cancer: cancer is confined to the gastric mucosa or submucosa, regardless of lymph node metastasis. Its maximum diameter of 5cm is generally less than 1cm in diameter, said small gastric cancer, gastric cancer less than 0.5cm said minor. Carcinoma in situ is not breaking the lamina propria of gastric cancer is also an early, but difficult to identify. ① type early gastric cancer in Japan: 1962 Japan's gross morphology of early gastric cancer is divided into three types: protruded, superficial and depressed type. A. uplift (Ⅰ type): surface of the tumor was nodular or polypoid bulge, clear boundary, about 2 times higher than the surrounding mucosa. B. Superficial (Ⅱ): the level surface of the tumor and not very large differences in the surrounding mucosa, foci relatively flat, no significant uplift and depression, according to their degree of uplift or depression was divided into three subtypes. Superficial elevated type (Ⅱ a): the tumor bulge height of not more than 2 times the thickness of the surrounding mucosa. Superficial flat-type (Ⅱ b): foci and the surrounding mucosa with high. No surface uplift or depression. Surface of the depressed type (Ⅱ c): foci compared with surrounding mucosa slightly depressed, depth of invasion less than mucosal thickness. C. depressed (Ⅲ): foci of significant depression, no more than submucosa. According to the characteristics of various types, but also the separation of mixed type, such as Ⅱ a + Ⅱ b, Ⅱ c + Ⅱ a, Ⅱ b + Ⅱ c, Ⅱ c + Ⅲ, Ⅲ + Ⅱ c, etc., shown in Figure 3. ② China type: China can be divided into three types, namely, protruding, polypoid cancer was elevated, more than 5mm above the gastric mucosa, pedunculated or sessile, primary or secondary to polyps. The Japanese classification of type Ⅰ, Ⅱ a and Ⅱ a type-type-based compound are classified in this type. Superficial gastritis, also known as type or flat type, only the very type Ⅱ b, according to lesion size range was divided into two subtypes, namely, localized (diameter <4cm) and diffuse type (diameter> 4cm), and drawn in the special type. Include a depressed type Ⅱ c, Ⅲ type and its main compound (Figure 4). More simple and practical advantages of this classification. According to statistics of China's most depressed early gastric cancer, followed by localized superficial, protruded at least. Some form of early gastric cancer in general different, said a special type of early gastric cancer. Include: A. Superficial diffuse type: Multi-proliferation in the mucosa, but also in the submucosal spread, diameter of more than 4cm. B. limitations of superficial type: superficial lesions, but limited to a diameter less than 4cm, earlier onset of lymph node metastasis. C. micro and small gastric cancer: foci <5mm were as small gastric cancer, mostly flat-type, <10mm are called small stomach, elevated type and depressed type more common, "a little cancer" refers to the endoscopic biopsy can be completely removed small foci. D. Multiple early gastric cancer: the same place on the stomach more than 2 separate foci of early, mostly multiple small gastric cancer. (2) of advanced gastric cancer: tumor tissues of advanced gastric cancer refers to more than submucosa. Once the breakthrough in the development of gastric cancer involving the submucosa and muscularis that is called when advanced gastric cancer. Foci can affect muscle, serosa and adjacent organs, more than a transfer. The general shapes of advanced gastric cancer, and often reflect their biological characteristics, Guchang unrecognized. 1923, Borrmann's classification method has been followed home and abroad, simple and practical. Borrmann1 type: elevated type, also known as polypoid carcinoma or bulky. Uplift to the stomach cavity, may have superficial ulceration or erosion, infiltration was not obvious, slow growth, late shift. Borrmann2 type: limited ulceration. Ulcers significantly, marginal uplift, infiltration was not obvious. Borrmann3 type: infiltrating the ulcer type. Infiltration was significantly associated with ulcers. Borrmann4 type: diffuse infiltrative. Infiltration of gastric wall layers and extensive lesions, ill-defined, mucosal folds disappeared, thickening and hardening of the stomach, it said, "Phascolosoma stomach." Type 4 to Type 3 and 2 in the more common type, type 1 is rare. In recent years, also proposed: Borrmann0 type, also known as superficial or flat infiltrating. China's sub-6: nodular fungating, discoid fungating, ulcerative limitations, and limitations of invasive ulcerative and diffuse infiltrative invasion (Figure 5). 2 Histopathology 1979 World Health Organization (WHO) histologic classification according divided into ① gastric adenocarcinoma will include: papillary adenocarcinoma, tubular adenocarcinoma, mucinous adenocarcinoma and mucinous carcinoma (signet ring cell carcinoma), and according to The degree of differentiation further divided into well differentiated, moderately differentiated and poorly differentiated three kinds; ② adenosquamous carcinoma; ③ squamous cell carcinoma; ④ carcinoid; ⑤ undifferentiated carcinoma; ⑥ unclassified carcinoma. China is divided into 4 types: ① adenocarcinoma: including papillary adenocarcinoma, tubular adenocarcinoma, mucinous adenocarcinoma (divided into well differentiated, moderately differentiated and poorly differentiated three kinds); ② mucinous carcinoma (signet ring cell carcinoma); ③ not differentiated cancer; ④ special type of cancer: adenosquamous carcinoma, squamous cell carcinoma, carcinoid, undifferentiated carcinoma and mixed carcinoma (Figure 6). 1965 Lauren according to gastric cancer histological characteristics of the gastric and intestinal type gastric cancer is divided into two types of diffuse-type gastric cancer: ① intestinal type, derived from intestinal metaplasia, better differentiation, gross morphology, mostly fungating; ② stomach type, originated in the gastric lamina propria, including undifferentiated carcinoma and mucinous carcinoma, poorly differentiated carcinoma, giant morphology, mostly ulcerative and diffuse infiltrative. Both in the organizational structure, epidemiology and prognosis are significantly different, this classification method is widely used. Foci in the same general type of organization and differentiation are often varying degrees of cancer tissue (cells) co-exist, and has evolved with the development of disease. According to international statistics, early gastric cancer histological features are as follows: ① the early differentiation of gastric cancer have a higher tendency to submucosal invasion with their degree of differentiation to mature direction; ② no mucinous adenocarcinoma of early gastric cancer abroad, National statistics are not always the case; ③ protruded more common high, medium differentiated papillary adenocarcinoma, tubular adenocarcinoma, undifferentiated carcinoma but not rare, depressed signet ring cell carcinoma is more common and differentiated adenocarcinoma, and papillary adenocarcinoma rare; ④ superficial localized well-differentiated tubular adenocarcinoma cancer more common; ⑤ extensive superficial 2 to 3 common histological type with the deposit, with well-differentiated tubular adenocarcinoma and poorly differentiated adenocarcinoma more, also see the nipple like adenocarcinoma and signet ring cell carcinoma. 3 Ultrastructure of gastric cancer of the ultrastructure of the current study received increasing attention. Has now shifted from a purely morphological study combined with the functionality, from advanced cancer to early cancer and precancerous lesions of the study. Incidence of gastric cancer, carcinogenesis, differentiation direction, functional status, and cancer classification and diagnosis of all play an important role. On the search for new specific markers such as enzymes, antigens, and morphometric analysis lend significance. 4 proliferation and metastatic spread (infiltration) and the transfer is an important biological characteristics of gastric cancer is an important factor affecting the efficacy, in-depth study has important clinical significance. Liotta and so on tumor cell invasion and metastasis is its basement membrane and extracellular matrix adhesion, degradation and movement of three-step process. The first in the primary site of tumor cells to adhere, and then from the original adhesion site, move to distant lymph nodes, capillaries, etc., and then cloned by adhesion to settle in the implantation and metastatic sites. In this process, cell adhesion molecules and proteolytic enzymes play an important role. Cell adhesion molecules are present in the cell membrane of a class of transmembrane glycoproteins, including the integration of system classes (integrins), calcium-dependent adhesion system class (cadherins), immunoglobulin gene super-Ig, selectin class (selectins) and CD44 and so on. In which E-cadherin (E-CD) is connected to the adhesion between epithelial cells, the major adhesion molecules, E-CD gene mutation or decreased expression can promote invasion of epithelial cells poorly and get power. CD44 is a cell surface adhesion molecules involved in cell - cell, cell - specific adhesion between the substrate, combined with hyaluronidase, 10 constitutive exons (CD44S) and 10 variant exons (CD44 -V1-10). The latter in the process of tumorigenesis and metastasis play an important role. And tumor invasion and metastasis of a variety of proteolytic enzyme, including metalloproteinases, thiol protease, aspartic acid and serine proteases and other enzymes. It has been reported, cathepsin (cathepsinB), also known as lysosomal thiol protease, in gastric cancer tissues strength and depth of invasion and lymph node metastasis were positively correlated. In addition, gastric stromal mast cells increased invasion and metastasis of gastric cancer was negatively correlated. (1) diffusion: the growth of cancer spread within the stomach is the main form of direct invasion, along the vertical direction to develop in depth, involving the muscle, serosa as well as surrounding organs such as the omentum, liver, pancreas, spleen, transverse colon, jejunum , such as the diaphragm or abdominal wall. Can also be spread along the horizontal direction, gastric cardia mucosa and submucosa via direct infiltration extended to the esophagus, stomach pylorus along the subserosa lymphatic spread to the duodenum. Ming will be divided into its growth and expansion of infiltrating type. Zhang is divided into three types: ① expansive proliferation or mass infiltration, pressure infiltration was ranked. ② diffuse infiltration or infiltrative proliferation. ③ nested infiltration, adenoid carcinoma nests scattered in the tissue infiltration, neither diffuse nor the formation of clumps. Late stage of gastric cancer, the same case often a way of non-proliferation. (2) lymph node metastasis: cancer metastasis through the lymphatic channels of the main transfer method. Practice has proved that with gastric cancer in different parts of its way to a certain law of lymph node metastasis. Therefore, the master distribution and lymph node metastasis, surgical treatment for gastric cancer is of great significance. Japan's "Surgery, Pathology of gastric cancer rules" under the stomach lymph node grouping, sub-station is more practical. To lymph nodes around the stomach is divided into 16 groups. ① the right cardiac lymph nodes; ② left cardiac lymph nodes; ③ lesser curvature lymph nodes; ④ greater curvature lymph nodes; ⑤ pyloric lymph nodes; ⑥ pyloric lymph nodes; ⑦ dry left gastric artery lymph nodes; ⑧ hepatic artery in the lymph nodes; ⑨ lymph nodes around the celiac artery; ⑩ splenic lymph nodes; ⑪ dry splenic artery lymph nodes; ⑫ hepatoduodenal ligament lymph nodes; ⑬ rear pancreatic lymph nodes; ⑭ mesenteric root lymph nodes; ⑮ lymph nodes around the colon in the artery; ⑯ lymph nodes around the abdominal aorta. According to the stomach, and in the next 3 parts per part of the lymphatic drainage from near and far are divided into 3 stations (Table 1). Range of surgical removal of lymph nodes to "D" to said first station lymph node removal surgery to D1 surgery to remove 2 points for the D2 lymph node surgery, surgery to remove lymph nodes in the first 3 points for the D3 surgical procedure. For example, gastric cancer, if the first station 3,4,5,6 remove lymph nodes, then the line gastrectomy as D1-type surgery. If the same cut points 1,7,8,9 group 2 lymph nodes, compared with D2-type surgery. If the lymph nodes also are removed 2,10,11,12,13,14,15,16 as D3-type surgery. If the D2-type resection on the basis of several sets of additional lymph node surgery, the third station called selective D3-type surgery. Other parts of the stomach and so on. Gastric wall layers, especially in the submucosa and subserosa rich lymphatic network. Therefore, it is easy to form the lymphatic channels diffusion transfer. Cancer cell proliferation in the lymphatic spread (more common in the nest the wild-type), you can walk off the float along the lymphatic vessels (more common in poorly differentiated adenocarcinoma or mucinous carcinoma Yayoi-type). Cause: ① lymphatic cancer lymphangitis. ② lymphatic cancer cells to swim outside of the formation of the stomach or the surrounding tissue (eg, omentum) metastases. ③ draining lymph nodes metastasis, mostly from near and far, from shallow and deep-order transfer. Lymph node metastasis and tumor size, depth of invasion, cell differentiation, gross type and primary site and other factors Jie relationship. In order to understand the laws of gastric cancer lymph node metastasis, lymphatic drainage of the stomach scholars conducted in-depth study of the direction. Rouvere the lymphatic drainage of the stomach is divided into four areas: ① gastric lesser curvature area (left gastric lymph nodes); ② liver, pylorus (right gastric lymph nodes); ③ liver, the right gastroepiploic Department (right gastroepiploic lymph nodes); ④ spleen area (left gastroepiploic lymph nodes). In practice, there are flaws. 1985, Japanese scholars to the surrounding lymph nodes at 18 distribution groups (Figure 7), and based on where the different parts of the gastric lymph nodes and direction of drainage channels, from near and far into three groups (Table 2). This sub-station group and the traditional partition method not only consistent but also more in-depth description of the stomach lymph drainage patterns. To more accurately reflect the universal law of lymph node metastasis in the stomach. There are some special diffusion transfer method: ① jump lymph node metastasis. ② peritoneal seeding. Cancer invasion to the serosa, the cancer cells in the peritoneal or leaching planting some organs, the formation of implanted cancerous peritonitis pelvic organ implanted transfer; ③ transfer of female genital mutilation. Metastatic ovarian cancer due to unclear, said the Krukenberg tumor, with signet-ring cell carcinoma of the common. Cervical metastasis rare. ④ The thoracic duct retrograde to the left supraclavicular lymph node (Virchow node) can also be transferred to the hepatic round ligament Cullen, the formation of abdominal wall metastatic cancer. (3) hematogenous metastasis: cancer occurred in the late, tumor infiltration damage blood vessels, cancer cells invade blood vessels, the occurrence of systemic spread, the most common metastatic sites were liver, lung, kidney, brain and other organs, followed by the pancreas, adrenal gland and bone, bone marrow and skin there. Rate of spread and metastasis of gastric cancer mode of behavior by their biological characteristics and impact of immune status is an important prognostic factor. (4), peritoneal: When the stomach serosa have been violated, the tumor cells can be shed, planted in the abdominal cavity and other organs of the wall on the serosal peritoneum, pelvic rectal and ovarian lacunae are often premises cultivation takes place, the transfer to ovarian cancer is called Krukenberg tumor. (5) the proliferation and metastasis of early gastric cancer: long-term mucosal carcinoma in the mucosa remain, mainly along the horizontal spread of intramucosal tubular adenocarcinoma mostly spread proliferative (discharge pressure of proliferation), signet ring cell carcinoma of the long-infiltrative proliferation of spread. Subject only to the underlying long-term spread, the depth of the spread of cancer is an important prognostic factor. Depth of invasion of early gastric cancer affecting lymph node metastasis is the most important factor. Mucosal carcinoma in lymph node metastasis is only 4% up to 18.9% of submucosal cancer. The deeper the lymph node invasion more chances. Second, the impact of tumor size is one of the factors, the larger the tumor the greater the chance of lymph node metastasis. More lymph node metastasis of poorly differentiated type. Early gastric cancer can also be blood transfer, mostly for liver involvement. According to statistics, more than to see blood metastasis following cases: ① elevated type carcinoma. ② small early gastric cancer. ③ submucosal cancer. ④ pyloric antrum cancer. ⑤ adenocarcinoma and papillary adenocarcinoma. ⑥ older men. 5 clinical staging (1) International Union Against Cancer staging criteria (1988) The staging is based on the depth of tumor invasion (T), lymph node involvement were (N) and distant metastasis (M) division , also known as the TNM staging method. Tis tumors confined to the epithelium, muscularis mucosa is not violated. T1 invasion and mucosa and submucosa. T2 and myometrial invasion or subserosa. T3 tumors have been through serosa. T4 Tumor invades adjacent organs or cavity structure extended to the esophagus or duodenum. No no lymph node metastasis. Less than 5cm from the tumor margin N1 lymph node metastasis. 5cm away from the tumor margin N2 lymph node metastasis, including the left gastric artery, common hepatic artery, splenic artery and lymph nodes around the celiac artery. M0 no distant metastasis. M1 distant metastasis, including near the common bile duct, pancreas, duodenum, mesentery, and aortic root, etc. of the transfer. (2) China's current staging of gastric cancer: TNM staging of gastric cancer in international law be modified on the basis of the development the following clinical and pathological staging of gastric cancer: T tumor depth of invasion. T1 regardless of tumor size, lesions confined to mucosa or submucosa. T2 invasion to the muscularis or subserosal. T3 through serosa. T4 invades adjacent structures or cavity extended to the esophagus, duodenum. N lymph node metastasis. N0 is no lymph node metastasis. Less than 5cm from the tumor margin N1 lymph node metastasis. N2 than 5cm from the edge of gastric cancer lymph node metastasis, including the left gastric, common hepatic, splenic and lymph node metastasis around the celiac artery. M distant metastasis. M0 no distant metastasis. M1 distant metastasis, lymph node metastasis including the first 12,13,14,16. Based on the above definition, the period of the division shown in Figure 8. (3) staging of gastric cancer in Japan (1998) with the biological characteristics of gastric cancer awareness and analysis of the prognosis of patients with gastric cancer, the staging of gastric cancer is still not well reflect the characteristics of gastric cancer, the Japanese scholar in 1998 to develop Statute of the 13th edition of gastric cancer Figure 9. ① stomach area is divided: the greater curvature, lesser curvature of the point of trisection draw length, connecting the greater curvature, lesser curvature of the corresponding point on the stomach is divided into (U), the (M), lower (L) three areas: 1 / 3 of areas, including cardiac and gastric, in 1 / 3 area of the body most of the stomach, the lower 1 / 3 of the area, including gastric antrum. If more than one area affected, all affected by involvement of the partition to be described, where the main tumor site listed in the front, such as LM or UML. Tumor invasion and esophagus or duodenum were recorded as E or D. ② depth of invasion (T): T1 tumor invasion and mucosal and / or mucosal muscle (M) or submucosal (SM). SM1 refers to the muscularis mucosa cancer over the lack of 0.5mm. SM2 refers to the muscularis mucosa cancer across more than 0.5mm. T2 tumor invasion and myometrial (M) or subserosal (SS). T3: tumor invasion through the serosa (SE). T4: Tumor invades adjacent structures (SI). Tx: depth of invasion is not clear. Penetrate the muscle size of the tumor can be extended to the omentum (or even to the stomach, colon, liver and stomach ligaments) and not covered in these structures penetrate the visceral peritoneum, the situation of the tumor as T2. If there is penetration of the visceral peritoneum, is set at T3. Invasion and the size of the omentum, esophagus and duodenum does not mean that T4 lesions, mucous membrane of the tumor extended to the esophagus or duodenum, grading from these locations to determine the maximum depth of invasion. ③ lymph node metastasis: primary tumor location according to the different regional lymph nodes can be divided into three stations. Specific parts of the tumor appeared occasionally a lymph node metastasis, distant metastasis as a sign (indicated by M); tumor invasion and the esophagus, NO19 ~ NO112 sub-station to be adjusted accordingly. ④ distant organ metastasis: A. liver metastasis (H): H0: no metastasis; H1: metastasis; Hx: not clear. B. peritoneal metastasis (P): P0: no peritoneal metastasis; P1: peritoneal metastasis; Px: not clear. C. peritoneal cytology (CY): CY0: benign / indeterminate cells; CY1: cancer; CYx: not for cytological examination. Note: The cytological diagnosis of "suspected malignant" should be set CY0. ⑤ other distant metastases (M): M0: no other transfer (even if there are peritoneal, liver or transfer of exfoliated cells). M1: In addition to peritoneal cytology outside the liver or distant metastasis. Mx: Distant metastasis is not clear.[Sign]
What are the symptoms of early gastric cancer?
clinical manifestations of early gastric cancer symptoms or only mild symptoms. When the clinical symptoms, the disease is already advanced. Therefore, be very wary of the early symptoms of gastric cancer, in order to avoid delay in diagnosis and treatment. 1 symptoms (1) early gastric cancer: With the progression of the disease, function of the stomach and the situation gradually changed the whole body, these symptoms are often nonspecific, can be hidden when, can be a long time. As abdominal distension and pain, dull pain, pain, nausea, loss of appetite, belching, and weight loss, etc.; small ulcer type (Ⅱ c and Ⅲ type) early gastric cancer may also have ulcer-like symptoms, was rhythmic pain, acid reflux, medical treatment can alleviate and so on. Some patients with gastric cancer and some benign lesions exist, or in some benign lesions, based on (such as chronic atrophic gastritis, peptic ulcer, etc.) to cancer, and these benign stomach disease symptoms long-standing, or repeated seizures, make it easier for patients and doctors to relax the vigilance of gastric cancer, and delay in diagnosis time. Some of the early gastric cancer can also be vomiting blood, black stools, or difficulty swallowing, symptoms and treatment. ① abdominal discomfort: is the most common cancer symptoms onset, about 80% of patients with this performance, and indigestion are similar, such as abdominal pain, usually beginning mild, and no regularity, can not be relieved after eating, gradually increased, for pain, dull pain. Part of the pain can have rhythm, especially gastric cancer is more obvious, even to eat or medication can be alleviated. Elderly pain slow, and many more bloating chief complaint. These symptoms are often not valued by patients, medical treatment, also easily mistaken for gastritis or ulcer disease. Therefore, middle-aged patients with any of the following conditions should be given further examination in order to avoid misdiagnosis: A. no previous history of stomach, but the recent unexplained abdominal discomfort or pain, the treatment fails; B. Past history of gastric ulcer, recent upper abdominal pain regularity of change, and increasing levels of increase. If symptoms have eased, but the hair of the short term there should also consider the possibility of gastric cancer, in a timely manner for further examination. ② loss of appetite or loss of appetite: loss of appetite and weight loss are common symptoms of gastric times, nearly 50% of gastric cancer patients have significant loss of appetite or loss of appetite symptoms, some patients because of eating too much can cause bloating or abdominal pain while eating their own limitations of. Anorexia and unexplained weight loss, it is likely that the initial symptoms of early gastric cancer, need for attention. Patients with early gastric cancer is generally no significant positive signs, the general condition of most patients in addition to weak, the only deep tenderness in the abdomen. (2) of advanced gastric cancer: gastric lesions from small to big, from shallow to deep, from the non-transferred to a transfer is a gradual process, so early, advanced and even there is no clear boundary between the late, not only that, the period symptoms are often a great cross between some patients with advanced disease have reached, but the symptoms are not yet clear, although at some of the more prominent early symptoms, but there are also some patients based on symptoms or complications of organ transfer of symptoms for treatment. According to statistical data of domestic common symptoms of advanced gastric cancer as follows: ① abdominal pain: When the stomach expand, especially in the violation of the pancreas infiltrating through serosa or transverse mesocolon, there may be persistent severe pain, radiation to the lower back. Very small number of cancer patients with perforated ulcer can be abdominal pain and signs of